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Activation of PAR₄ Induces a Distinct Actin Fiber Formation via p38 MAPK in Human Lung Endothelial Cells

Masakazu Fujiwara, Enjing Jin, Mohammad Ghazizadeh and Oichi Kawanami

Department of Molecular Pathology, Nippon Medical School, Graduate School of Medicine, Institute of Gerontology, Kanagawa, Japan

Correspondence to: Oichi Kawanami, MD, PhD, Department of Molecular Pathology, Nippon Medical School, Graduate School of Medicine, Institute of Gerontology, 1-396 Kosugi-cho, Nakahara-ku, Kawasaki, Kanagawa, Japan. E-mail: kawanami{at}nms.ac.jp

Protease-activated receptors (PARs) are multifunctional G protein–coupled receptors. Among the four existing PARs, PAR₄ is preferentially expressed in the human lung tissue. However, the function of PAR₄ has not been defined in the lung endothelial cells. Because PAR₁-mediated cellular effects are deeply related to the morphological changes, we focused on the actin fiber and p38 mitogen-activated protein kinase (MAPK) signaling involved in actin polymerization to elucidate the role of PAR₄. RT-PCR and Western blot analyses identified PAR₄ expression in human pulmonary artery endothelial cells and in human microvascular endothelial cells from lung. We then examined the changes in actin fibers in endothelial cells treated with PAR₄-activating peptide. PAR₁-activating peptide was used for comparison. Activation of PAR₄ and PAR₁ by their corresponding peptides induced actin fiber formation; however, the actin filaments were broadly bundled in PAR₄ as compared with the ringlike actin filaments in PAR₁ activation. Correspondingly, the magnitude of p38 MAPK phosphorylation was different between cells treated with PAR₄ and PAR₁, with PAR₄-activating peptide showing a significantly higher sensitivity to p38 MAPK inhibitor, SB203580. Taken together, these results demonstrate that activation of PAR₄ results in the formation of actin fiber distinct from that by PAR₁ activation, suggesting PAR₄ may play specific roles in the lung endothelial cells. (J Histochem Cytochem 53:1121–1129, 2005)

Key Words: pulmonary endothelial cells • G protein–coupled receptors • protease-activated receptor • thrombin • actin • p38 MAPK

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